Connexin () involves in the regulation of various physiological functions of tissue by forming a channel, a gap junction which allows direct cell-cell communication, between adjacent cells. The effect of a single subcutaneous treatment of estradiol benzoate (EB) or flutamide (Flu) at the weaning age on the expression of isoforms in the adult caput epididymis was evaluated in this research. Using quantitative real-time PCR analysis, a low-dose of EB [0.015 μg/kg body weight (BW)] caused significant decreases of 30.3, 32, 40, 43, and 45 mRNA levels and no change of 26, 31, 31.1, 37 transcript levels. The treatment of a high-dose EB (1.5 μg/kg BW) resulted in reduced expression of 30.3, 31, 43, and 45 but increased expression of 37 and 40. Expression of all isoforms examined, except 31, was significantly increased by the treatment of a low-dose Flu (500 μg/kg BW). However, the treatment of a high-dose Flu (5 mg/kg BW) led significant expressional suppression of 30.3, 31, 31.1, 32, 40, 43, and 45 but an increase of 37 transcript level. With the comparison of previous findings, the expression of isoforms in the adult epididymis after the exposure to EB or Flu is likely differentially regulated in regional-specific and/or exposed postnatal age-specific manner.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5769132 | PMC |
http://dx.doi.org/10.12717/DR.2017.21.4.379 | DOI Listing |
Am J Physiol Renal Physiol
December 2024
Molecular Physiology Unit, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, and Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Tlalpan, Mexico City, 14080 Mexico.
The field of the with no lysine kinases (WNKs) regulation of the thiazide-sensitive NaCl cotransporter (NCC) began at the start of the century with the discovery that mutations in two members of the family, WNK1 and WNK4, resulted in a condition known as Familiar Hyperkalemic Hypertension (FHHt). Since FHHt is the mirror image of Gitelman's syndrome that is caused by inactivating mutations of the SLC12A3 gene encoding NCC, it was expected that WNKs modulated NCC activity and that the increased function of the cotransporter is the pathophysiological mechanism of FFHt. This turned out to be the case.
View Article and Find Full Text PDFAACE Clin Case Rep
July 2024
Division of Endocrinology, Metabolism, and Molecular Medicine, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Background/objective: Fanconi-Bickel Syndrome (FBS) is an inherited disorder of glucose metabolism resulting from functional loss of glucose transporter 2 characterized by fasting hypoglycemia oscillating with postprandial hyperglycemia. Dysglycemia treatment strategies during FBS pregnancy have not been reported, and insulin therapy carries significant risk due to fasting hypoglycemia in FBS. We report for the first time: (1) glycemic profiles obtained via continuous glucose monitoring (CGM), (2) CGM-guided strategies for cornstarch and nutritional therapy for fasting hypoglycemia and postprandial hyperglycemia, respectively, and (3) placental glucose transporter 2 isoform expression in a pregnant individual with FBS.
View Article and Find Full Text PDFTurk J Med Sci
December 2024
Department of Microbiology, Faculty of Medicine, Ankara University, Ankara, Turkiye.
Background/aim: The p53 protein, a crucial tumor suppressor, governs cell cycle regulation and apoptosis. Similarly, p63, a member of the p53 family, exhibits traits of both tumor suppression and oncogenic behavior through its isoforms. However, the functional impact of ΔNp63β, an isoform of the p63 protein, on human glioma cancer cells like T98G cells remains poorly understood, representing the novelty of this study in the current literature.
View Article and Find Full Text PDFAm J Pathol
December 2024
Division of Gastroenterology and Hepatology, Stanford University, Palo Alto, California; Palo Alto VA, Palo Alto, California. Electronic address:
Mitochondrial maladaptation and dysfunction contribute to the progression of metabolic dysfunction-associated steatohepatitis (MASH). The authors recently implicated the induction of Shc in progressive MASH during aging and the cytoplasmic p52Shc isoform in the activation of redox enzyme NOX2. The mitochondrial Shc isoform p46Shc was shown to repress acetyl-coenzyme A acyltransferase 2 (ACAA2) in vitro.
View Article and Find Full Text PDFSci Rep
December 2024
Department of Pharmaceutical Sciences, Northeast Ohio Medical University, Rootstown, OH, USA.
Carbapenem-resistant Acinetobacter baumannii (CRAb) is an urgent bacterial threat to public health, with only a few treatment options and a > 50% fatality rate. Although several resistance mechanisms are understood, it is still impossible to predict which mutations are most likely to occur. Here, we demonstrate that independent samples of Ab, exposed to different carbapenems with escalating concentrations, show concentration- and carbapenem-dependent trends in β-lactamase-isoform expression.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!